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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lead toxicity causes hematological, gastrointestinal, and neurological dysfunction in adults and children. Symptoms are usually noted with blood lead greater than 1.93 mumol/L. Severe or prolonged exposure may also cause chronic nephropathy, hypertension, and reproductive impairment. Lead inhibits enzymes; alters cellular calcium metabolism; stimulates synthesis of binding proteins in kidney, brain, and bone; and slows nerve conduction. Less severe exposure to lead, designated by blood lead levels of 0.48-0.96 mumol/L, has been implicated in poor pregnancy outcome, impaired neurobehavioral development, reduced stature in young children, and higher blood pressure in adults. Biochemical and systemic effects of high and low level lead toxicity are described. Dust, water, and paint chips are still major sources of lead but lead from folk remedies, cosmetics, food supplements, food preparation utensils, and improperly prepared infant formula has caused epidemic and sporadic severe lead toxicity. Screening for pediatric low level lead exposure requires measurement of blood lead.
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PMID:Perspectives on lead toxicity. 829 7

Lead is considered a pathogenic factor of atherosclerosis and arterial hypertension, which are main risk factors of cerebrovascular disease. The brain microvasculature preferentially accumulates lead and its function is sensitive to its toxic effect. Influence of inorganic lead-exposure (20 mg/kg-I group, 40 mg/kg II group) for 10 days on local cerebral blood flow (lCBF) in hypothalamus (HYP) and cerebral cortex (CTX) of rabbits was studied by means of the hydrogen clearance method. Corresponding results were compared to sham operated group (III group). During lead-exposure lCBF was reduced in both investigated regions. The reduction of lCBF in HYP was reduced in both investigated regions. The reduction of lCBF in HYP was 12.9% (P < 0.05) in I and 19.9% (P < 0.001) in II group; corresponding changes in CTX were -16.9% (statistically non-significant -N) in I and 1.4% (NS) in II group. Present finding suggest that inorganic lead induces cerebral microvascular dysfunction with following changes in lCBF. These alteration have a biphasic character Although these disturbances reveal a tendency towards normalization, it is possible to presume that higher concentrations of ingested lead cause more severe injury to endothelium of brain microvasculature.
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PMID:Changes of local cerebral blood flow concomitant to lead-exposure in adult rabbits. 875 Jan 16

Lead intoxication in human beings has been documented since the second century B.C. Renal disease, hypertension, and gout have all been linked to lead by strong circumstantial evidence. Both acute and chronic nephropathy can occur as a result of lead poisoning. Acute renal failure develops following acute lead intoxication and is often associated with gastrointestinal, neurologic, and hematologic disorders. Both blood and urinary laboratory abnormalities are associated with acute intoxication and are often diagnostic. Chronic lead nephropathy, a chronic tubulointerstitial nephritis on biopsy, occurs in the setting of long-term lead exposure and is often associated with hypertension and gout. Diagnosis of chronic lead nephropathy is more difficult since the laboratory abnormalities seen with acute lead intoxication are not present with chronic lead exposure. The typical clinical picture and the exclusion of other causes of renal disease allow the diagnosis of chronic lead nephropathy to be made. Evaluation of lead stores by either the calcium disodium edetate (EDTA) mobilization test or K-x-ray fluorescence are helpful in clinching the diagnosis. Treatment with EDTA lead mobilization is effective for acute lead poisoning while avoidance of further lead exposure prevents recurrence of lead intoxication. Treatment of chronic lead nephropathy with EDTA lead mobilization is useful if renal failure is modest; however, EDTA mobilization is of no benefit in patients with more severe renal insufficiency.
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PMID:Lead and the kidney: nephropathy, hypertension, and gout. 890 77

Chronic exposure to low levels of lead results in sustained hypertension (HTN) in humans and experimental animals. The mechanism of lead-induced HTN remains unclear. We investigated the possible role of reactive oxygen species (ROS) and their impact on nitric oxide (NO) metabolism in lead-induced HTN. Male Sprague-Dawley rats were treated with lead (100 ppm in drinking water) for twelve weeks. They were then treated with either the potent antioxidant, lazaroid (des-methyl-tirilazad, 5 mg/kg i.p., twice daily) (Pb-Lz group) or placebo (Pb group) for two weeks and monitored for an additional two weeks. A group of normal animals served as controls (N = 6 in each group). Lead administration resulted in marked HTN together with a significant rise in plasma concentration of lipid peroxidation product, malondialdehyde (MDA, reflecting increased ROS generation) and a twofold reduction in urinary excretion of NO metabolites, that is, total nitrates and nitrites (NOx). Lazaroid therapy led to prompt normalization of blood pressure, plasma MDA and urinary NOx. In contrast, blood pressure and plasma MDA remained elevated, and recovery of urinary NOx excretion was slow with placebo therapy. No significant difference was found in creatinine clearance between the study groups during the observation period. Thus, chronic lead exposure resulted in marked HTN coupled with increased ROS production and decreased urinary NOx excretion. Administration of the potent antioxidant, lazaroid, abrogated HTN and reversed the abnormalities of plasma MDA and urinary NOx excretion, thus supporting the role of ROS in lead-induced HTN in this model.
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PMID:Altered nitric oxide metabolism and increased oxygen free radical activity in lead-induced hypertension: effect of lazaroid therapy. 932 43

Administration of 100 ppm lead acetate daily for 3 months caused hypertension in Sprague-Dawley rats, with reversal by treatment with 2,3-dimercaptosuccinic acid (DMSA) (0.5% for 2 weeks). Animals from each group were infused sequentially in 30-min intervals with saline (S), L-arginine (Arg), Arg+ superoxide dismutase (SOD), S, and sodium nitroprusside (SNP). Baseline mean blood pressure (MBP) was elevated in lead-treated animals (Pb) compared to that in controls(C), returning toward normal after DMSA (105 +/- 2 mmHg, C, vs 149 +/- 2, Pb, and 124 +/- 1, DMSA, P < 0.001). Infusion of Arg caused a fall in MBP in all animals, normalizing the MBP in Pb-treated animals. SNP caused a greater fall in MBP in all groups of animals, normalizing the MBP in Pb. Measurement of urinary nitrite + nitrate (NOx) by chemiluminescence revealed at baseline a reduced level in Pb, restored to normal by DMSA (6.6 +/- 1.5 nmol/min/100 g BW, C, vs 3.3 +/- 1.7, Pb, P < 0.05, vs 5.8 +/- 2.6, DMSA, P = NS). Infusion of arginine increased urinary NOx in all groups, but to a lesser degree in Pb and DMSA. Assay of plasma malondialdehyde (MDA) by HPLC, as a measure of reactive oxygen species (ROS), was elevated at baseline in Pb, reduced by DMSA (3.6 +/- 0.4 mumol/L, Pb, vs 1.9 +/- 0.2, C, and 1.9 +/- 0.3, DMSA, P < 0.01). In the Pb group, SOD resulted in a significant fall in MDA (2.0 +/- 0.3 mumol/L, SOD, vs 3.1 +/- 0.1, Arg, P < 0.01), but no further fall in MBP or increase in urinary NOx. Thus, hypertension in lead-exposed animals is related to both diminished NO and increased ROS. The elevation in MBP can be ameliorated by additional NO through infusion of substrate arginine or by treatment with the ROS scavenger, DMSA. Lead-exposed animals show enhanced MBP sensitivity to the NO donors, Arg and SNP, but no further response to SOD, despite a reduction in MDA to normal. We speculate that lead-induced hypertension may be caused by one species of ROS which enhances vascular reactivity, and that provision of additional NO acts to scavenge the ROS and/or acts directly as a vasodilator.
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PMID:Lead-induced hypertension. II. Response to sequential infusions of L-arginine, superoxide dismutase, and nitroprusside. 951 65

In a comparative ECG study of 288 hypertensive and 340 normal Nigerians, the following observations were made: a) The QRS voltage is high in normal Negroes but becomes significantly higher in hypertension (HBP). This suggests that the voltage criteria being used for LVH in Caucasians are not applicable to Negroes. b) The T wave amplitude diminishes in HBP culminating in ST-T flattening or down-sloping ST-segment with asymmetric T inversion, so called "Strain pattern" c) The Washington code for LVH (Rx amplitude > 2 mV, Rx + Rz > 3.4 mV and Rz duration > 0.06 sec) achieved a cumulative sensitivity of 70.7% with 83.5% specificity in males. In females, Rx > 2 mV, Rx + Rz > 2.6 mV and Rz duration > 0.07 sec. achieved a sensitivity of 71.6% with 92.4% specificity. d) In the 12-Lead system, RI > 1.1 mV Sv2 + Rv5 > 4.5 mV (male), Sv2 + Rv5 > 4.2 mV (female) and Tv6 < -0.05 mV achieved a cumulative sensitivity of 74.3% with 87.6% specificity in males; 72.3% with 91.8% respectively in females. It is suggested that further studies are required to authenticate these criteria for LVH in Negroes.
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PMID:The orthogonal and 12 lead ECG in adult negroes with systemic hypertension: comparison with age-matched control. 981 84

The article covers some results of complex sanitary, hygienic, clinical, functional and laboratory examinations of individuals working in main shops of storage battery production where lead and its inorganic compounds are principal occupational hazards. Lead and its compounds harm human health, being risk factors for vegetoneurosis and arterial hypertension. Hemodynamic studies using integral rheography revealed hemodynamic type of circulation, increase of general and peripheral vascular tone. The main causes of hemodynamic disorders are influence of lead compounds on autonomous nervous system, prevalence of the parasympathetic section and metabolic disorders in myocardium.
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PMID:[Several aspects of occupational effects of lead compounds on the cardiovascular system]. 991 47

Sally Hart Wilson is one of several lawyers who, on behalf of the Center for Medicare Advocacy, have filed a class-action suit seeking better protections for Medicare beneficiaries in HMOs. The experience of the lead plaintiff (one of 15) in Grijalva v. Shalala illustrates the down side of Medicare HMOs, says Ms. Wilson. Grigoria Grijalva, 71, an enrollee with diabetes, hypertension, congestive heart failure, anemia, and a uremic bladder, complained to her physician about pain in her foot. But the physician's treatment was inadequate, the complaint alleges, and as a result her right leg was amputated. In subsequent years, the lawsuit says, the HMO denied necessary skilled nursing home days and skilled home health services and never sent a notice of denial or a description of her appeal rights, as Medicare requires.
Health Syst Lead 1995 Jun
PMID:Another view of Medicare HMOs: not always what the doctor ordered. Interview by Meg Matheny. 1014 90

Lead exposure is considered to be a risk factor of cardiovascular disease. To investigate the relationship between lead and cardiovascular disease/hypertension in lead exposure, beta-adrenergic system is explored in this study. We address three topics in this study: (a) the relationship between beta-adrenergic receptor and lead level in heart, aorta, and kidney of lead-exposed rats; (b) the relationship between beta-adrenergic receptor in heart, aorta, kidney, and blood pressure in lead-exposed rats; and (c) the change of cyclic AMP level in heart, aorta, and kidney of rats with different lead levels. Wistar rats were chronically fed with 2, 1, 0. 5, 0.1, 0.05, and 0.01% lead acetate and water for 2 months. Plasma catecholamine level was measured by high-performance liquid chromatography. Radioligand binding assay was measured by a method that fulfilled strict criteria of beta-adrenoceptor using the ligand [(125)I]iodocyanopindolol. Cyclic AMP (cAMP) level was determined by radioimmunoassay. The levels of lead were determined by electrothermal atomic absorption spectrometry. The results showed that increased plasma norepinephrine level, decreased aorta beta-adrenergic receptor and cAMP, and increased kidney beta-adrenergic receptor and cAMP contributed to the elevation of blood pressure in lead-induced hypertension. The decrement of beta-adrenoceptor and cAMP in heart resulted in decreased contractility in heart.
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PMID:The change of beta-adrenergic system in lead-induced hypertension. 1076 25

Metals, particularly heavy metals such as lead, cadmium, and arsenic, constitute significant potential threats to human health in both occupational and environmental settings. Lead exposure is of particular concern because of ongoing exposure to thousands of workers in the US and recent research indicating that asymptomatic lead exposure can result in chronic toxicity manifestations, such as hypertension, kidney impairment, and cognitive disturbances. Mercury is neurotoxic, even at the relatively low levels of exposure seen in dentists' offices. Arsenic is clearly carcinogenic, and cadmium is now being recognized as a contributor to osteoporosis. This article reviews these and other issues of concern in the practice of primary care.
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PMID:Exposure to metals. 1107 95


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